E histolytica infection

Entamoeba histolytica infection (E. histolytica infection) Description, Causes and Risk Factors: Entamoeba histolytica: A species of ameba that is the only distinct pathogen of the genus, the so-called “large race” of Entamoeba histolytica, causing tropical or amebic dysentery in humans and also in dogs (humans are the reservoir for canine infections). In humans, the organism may penetrate the epithelial tissues of the colon, causing ulceration (amebic dysentery); in a small proportion of these cases, the organism may reach the liver by the portal bloodstream and produce abscesses (hepatic amebiasis); in a fraction of these cases it may then spread to other organs, such as the lungs, brain, kidney, or skin and frequently be fatal. Causes and Risk Factors: E. histolytica infection can occur when a person, Puts anything into their mouth that has touched the feces (poop) of a person who is infected with E. histolytica.
  • Swallows something, such as water or food, that is contaminated with E. histolytica.
  • Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
  • People who have traveled to tropical places that have poor sanitary conditions.
  • Immigrants from tropical countries that have poor sanitary conditions.
  • People who live in institutions that have poor sanitary conditions.
  • Men who have sex with men.
One theory of E. histolytica's origin of virulence is coincidental evolution. Host cells may have recognition patterns similar to those of enteric bacteria that the parasite has evolved to identify. Entamoeba histolytica has been shown to preferentially phagocytose cells coated with collections, C-type lectins involved in recognition of ligands that are common to both bacteria and apoptotic cells. An e?ective hijacking of the host's own innate immune system to increase phagocytosis may have led to an invasive phenotype. In further support of this theory, researchers have shown that several signaling proteins required for Entamoeba histolytica's virulence are also utilized to kill and phagocytose bacteria. Another seemingly plausible explanation is that Entamoeba histolytica's invasive phenotype arose in response to host defense mechanisms. Directed apoptosis and subsequent phagocytosis may serve to limit host in?ammatory mechanisms by suppressing necrosis and subsequent Th1-type immunity. Cysteine proteases that are known to degrade host extracellular matrix also protect Entamoeba histolytica from complement, secretory IgA, and serum IgG. While the evolutionary basis behind virulence is uncertain, the mechanism behind virulence is slowly becoming clearer. Invasion by Entamoeba histolytica is strongly correlated with the parasite's capacity to kill and phagocytose host cells. The function of this review is to highlight some of the recent advances in understanding the mechanism of cell killing and phagocytosis, and to place these ?ndings in the context of previous knowledge. For the purpose of this review, cell killing and phagocytosis have been organized in a sequential model involving (i) adherence to the host cell surface, (ii) contact-dependent cell killing, (iii) initiation of phagocytosis, and (iv) engulfment. In the US, E. histolytica infection is most often found in immigrants from developing countries. It also is found in people who have traveled to developing countries and in people who live in institutions that have poor sanitary conditions. About 10% of the world's population is infected with E. histolytica infection. About 90% of infected people are asymptomatic, but the disease causes 50,000-100,000 deaths per year. Symptoms:Entamoeba histolytica The symptoms often are quite mild and can include loose stools, stomach pain, and stomach cramping. Amebic dysentery is a severe form of E. histolytica infection associated with stomach pain, bloody stools, and fever. Rarely, E. histolytica invades the liver and forms an abscess. Even less commonly, it spreads to other parts of the body, such as the lungs or brain. Diagnosis: Diagnosis of E. histolytica infection can be very difficult. One problem is that other parasites and cells can look very similar to E. histolytica when seen under a microscope. Therefore, sometimes peopleare told that they are infected with E. histolytica even though they are not. Entamoeba histolytica and another amoeba, Entamoeba dispar, which is about 10 times more common, look the same when seen under a microscope. Unlike infection withE. histolytica, which sometimes makes people sick, infection with E. dispar never makes people sick and therefore does not needto be treated.Your health care provider will ask you to submit stool samples. Because E. histolytica is not always found in every stool sample, you may be asked to submit several stool samples from several different days. Laboratory findings include leukocytosis without eosinophilia in 80% ofcases, mild anemia in more than half, elevated alkaline phosphataselevels in 80%, elevated transaminase levels in more aggressive disease,mild elevation of serum bilirubin level, and a high erythrocytesedimentation rate. Abdominal ultrasonography, computedtomography (CT), and magnetic resonance imaging (MRI) are all excellentfor detecting liver abscesses, but cannot distinguish amebic frompyogenic abscesses. Anti-amebic antibodies are present in up to 99% of patients who havebeen symptomatic for over a week.Serological examination should berepeated a week later in those with negative test on presentation. Thegalactose lectin antigen is present in the serum of 75% of subjects withamebic liver abscess, and may be particularly useful in patientspresenting acutely, before an IgG serum anti-amebic antibody responseoccurs.Aspiration of the abscess is occasionally required to rule out apyogenic abscess. Aspiration of amebic liver abscess yields an anchovy-paste-like material that lacks white blood cells (WBCs) due to lysis by theparasite. Amebas visible in the abscess fluid in a minority of patientswith amebic liver abscess. Fewer than half of patients with amebic liverabscess have parasites detected in their stool by antigen detection. Treatment: Several antibiotics are available to treat E. histolytica infection. Treatment must be prescribed by a physician. You will be treated with only one antibiotic if your E. histolytica infection has not made you sick. You probably will be treated with two antibiotics (first one and then the other) if your infection has made you sick. Drug therapy of invasive E. histolytica infection is different from that of non-invasive infection. Asymptomatic infection should be treated because of its potential to progress to invasive disease. Luminal agents — such as paromomycin, iodoquinol, or diloxanide furoate — that are not absorbed are best suited for such a therapy. Metronidazole, a nitroimidazole, is the mainstay of therapy for invasive E. histolytica infection. Tinidazole has also recently been approved by the US Food and Drug Administration (FDA) for intestinal or extraintestinal E. histolytica infection. Other nitroimidazoles with longer half-lives — i.e. secnidazole and ornidazole are currently unavailable in the US. Nitroimidazole therapy leads to clinical response in ~90% of patients with mild to moderate E. histolytica infection. Nitroimidazole therapy does not eradicate the intraluminal parasites, and should be followed by treatment with a luminal agent such as paromomycin or diloxanide furoate to prevent a relapse. Dehydroemetine has been used successfully, but is not preferred due to its potential myocardial toxicity. Surgical intervention is required for acute abdominal pain due to perforated amebic colitis, massive gastrointestinal bleeding, or toxic megacolon. Surgical attempts to correct amebic bowel perforation or peritonitis should be avoided, although some patients may benefit from peritoneal lavage. Unlike pyogenic liver abscess, amebic liver abscess generally responds to medical therapy alone, and drainage is seldom necessary. The indications for drainage of amebic liver abscess include presence of left-lobe abscess, size >10cm in diameter, impending rupture, and abscess that does not respond to medical therapy within three to five days. Imaging-guided percutaneous treatment (needle aspiration or catheter drainage) has replaced surgical intervention as the procedure of choice for reducing the size of an abscess. NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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